Heath

1. Veterinary Toxicology and
Chemotherapy
Submitted by: Group 5
Submitted to : Mam Tehreem Fayyaz
Plants and Animal Poison

2. Plant Poisons
 Abrus precatirus (RATTI or GANGCHI):
Poison: It contains poisonous toxin, Abrin, a substance very similar to ricin of castor oil.
About 60 g of seed is sufficient to kill a horse. Abrin protein base toxin type 2 ribosomes
inactivating protein. Inhibit protein formation. Without protein cell not survive.
Toxicokinetic
Degrades in the GIT and absorb in circulatory system or blood. Even minute amount absorb
in circulatory system could cause death. Molecules is excreted via kidney in urine after it
undergoes proteolytic cleavage ( hydrolysis of a peptide bond in a protein substrate by
enzyme proteases.)
Symptoms: It produce violent purgation, incoordination and paralysis. High fever is first
noted and then hypothermia occurs.
Treatment: includes SC injection of arecoline hydrobromide. Purgatives like magnesium or
sodium sulphate can also given.

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 Aconitum nepellus (MOHRI, MITHA ZEHAR, ACONITE):
Poison: All parts of the plant especially the root is extremely poisonous which contain
aconitine and other alkaloids; maximum content is found just before flowering. About 5 g
of the dried root are lethal to dog and 300-400 g of the fresh root are lethal to horse.
Aconitine previously used as antipyretic and analgesic block the conduction of voltage
sensitive sodium channels in cardiac and nerve tissue. Aconitine first stimulate and than
depresses CNS metabolized by cytochrome p450 in liver.
Symptoms: It acts as a gastrointestinal irritant, produces respiratory paralysis, ventricular
fibrillation. Include attempted vomiting, colic, bradycardia, low respiratory rate, muscular
weakness, paralysis and dilated pupils. Death is due to asphyxia.
Treatment: There is no specific antidote. Give heart stimulants like digitalis, keep the
animal warm and rub the animal to increase the circulation.

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Aesculus indica (KNOR, BYCHEYE):
The plant is found on the side of rivers and streams. Its seeds are
poisonous to cattle and horses but cooking destroys the poison.
Aesculin Mechanism is uncertain.Neurotoxic at low dosage and
hemolytic at higher dosage.
Symptoms: CNS sedation occurs and the animal looks lazy and
weak. Then shivering and paralysis occurs and the mucous
membranes of the eye and intestine are inflamed.
Treatment: Treatment is symptomatic.

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Anamirta cocculus (KAKMARI or KAK PHUL):
Poison: The kernels of this plant contain picrotoxin.
Symptoms: In dogs and cats, there is vomiting and in other animals
convulsive seizures are produced. There is rolling on the ground and
muscular spasms.
Picrotoxin Act on synapse and it act as a non competitive antagonist for
GABA receptors. Prevent ion flow through chloride channel. GABA
enhancing drugs use to treat it.
Treatment: Treatment is symptomatic. Injection of phenobarbitone, chloral
hydrate or magnesium sulphate may prove useful.

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 Solanum nigrum (Nightshade plant)
 Solanum tuberosum (Potato, Aaloo)
Poison: All plants contain glycoalkaloids, solanine. All parts of S. nigrum are dangerous but
alkaloids are concentrated in berries. Inn S.tuberosum high concentration of alkaloids are
present in eyes, skin and the young green sprouts. In animal models, solanine acts as a
cardiac glycoside and inhibits cholinesterase activity ( acetylcholine increases in the body
due to inhibition of AchE enzyme). 2 to 5 mgkg of BW can cause toxic symptoms, doses of
3 to 6 mgkg of BW can be fatal.
Symptoms: The toxin includes gastrointestinal symptoms vomiting, salivation, diarrhea
with potential impact on central nervous system. Symptoms may be prolonged, depending
on the severity of the poisoning.
Treatment: Fluid and electrolyte replacement, purgatives, CNS stimulants (strychnine,
dextroamphetamine) and supportive care is the general approach to symptoms of poisoning.

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 Calotropis gigantea (AAK, MADAR):
Poison: The leaves contain a milk-like fluid which is poisonous, It contain
calotropin, uscharin, calotoxin that are toxic glycosides. The toxicity of cardenolides
is due to their ability in inhibiting the Na K ATPase pump ( due to influx of Ca ion
in the nerve cell more Ach releases at the synapse) and show cholinergic effect . It is
an irritant . The fatal dose is uncertain.
Symptoms: The juice produce an acrid, bitter taste and burning pain in stomach,
stomatitis, respiration is slow and dyspnea, vomiting in small animals, salivation,
animal falls down on the ground due to muscular spasms, collapse and death.
Treatment: Treatment include administration of a purgative or stomach wash and
then given symptomatic treatment. On mouth lesions, boroglycerine should be
applied and chloral hydrate( as a sedative) may be given to control spasm.

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 Croton tiglium (CROTON SEEDS, JAMAL-GOTA):
Poison: The seeds contain crotin, a toxalbumin. The oil contain a powerful
vesicating resin composed from croton oleic acid which is able to cause
toxicity to the digestive tract ( vesicles forms in the GIT and damage GIT wall)
and cause diarrhea. 4 to 5 crushed seeds or 20 drops of oil is fatal dose.
Symptoms: There is hot burning pain from mouth to stomach, salivation,
vomiting purging with bloody stool, dizziness, recumbent, collapse and death.
Treatment: Stomach wash, demulcents and symptomatic treatment.

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 Datura stramonium ( DHATTURA)
D.fastuosa (Kala dhattura)
D.fastuosa var alba (safed dhattura)
Atropa belladona (angur shefa, Belladona)
These plants contain Atropine which which is antagonist of acetylcholine at
mascarinic receptor and produces anti cholinergic effect.
Symptoms: Animals show mydriasis, impaired vision, rapid pulse, anorexia,.
Cows show severe nervous symptoms. All the secretions are dried, animal feels
great difficulty in swallowing and is paralysed.
Treatment: Treatment includes removal of undigested plant by stomach tube or
purgation. Antidote for atropine poisoning is physostigmine ( inhibits cholinestrase
enzyme activity and show cholinergic effect) or pilocarpine ( antagonist of
Atropine and show cholinergic effect)

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 Digitalis purpurea (FOX-GLOVE):
Poison: Its leaves and seeds contain a mixture of glycosides which includes
digitoxin, gitoxin, and gitalin. Digoxine is obtained from the leaves of Digitalis
lanata. Dog, cat, and horse are quite susceptible while ruminants are relatively
resistant by oral route.
Symptoms: Mild poisoning symptoms include depression, vomiting, diarrhoea,
and bradycardia. Cardiac irregularities occur. Heart block may occur when the
heart stops with auricles dilated and full of blood and ventricles contracted and
empty. In Animals are anaemia and stomatitis is also observed.
Treatment: Treatment include passing a stomach tube or giving emetics and
purgatives. Atropine is given to check excessive vagal stimulation. It also includes
administration of cobalt pellets, blood transfusion, glucose saline drips and ferrous
sulphate in the feed.

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 Tobacco (TAMBAKOO):
Poison: The leaves contain an alkaloid, nicotine. Nicotine is one of the most toxic
substances and is also absorbed from the skin. Minimal lethal dose for horse is 0.2-
0.3 g, sheep, 0.1-0.2 g, dog and cat, 0.02-0.1 g.
Symptoms: In acute poisoning, there is marked excitement, rapid respiration,
salivation, irritation or buccal and pharyngeal mucosa, diarrhoea, and vomiting. Then,
depression occurs with incoordination, rapid pulse, shallow and slow respiration,
coma, flaccid paralysis and death due to respiratory paralysis.
Postmortem lesions: At post mortem, cyanosis, engorgement of SC vessels and poor
coagulation of blood.
Treatment: Treatment is not usually successful in acute cases. In less severe cases,
artificial respiration and stimulants like coramine, leptazole, and strychnine should be
tried. Strong tea or SC injection of caffeine citrate (1 g) and strychnine (67 mg) to a
cattle may prove useful.

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 Ricinus communis (CASTOR-OIL PLANT, ARIND):
Poison: Castor seeds contain the active poison, ricin. Since it is a
protein, antibody formation occurs.
Symptoms: In horses, the dullness followed by incoordination,
sweating, and tetanic convulsions. Heart heat is such that it shakes the
entire body. All animals show pro fuse diarrhoea but no blood in
faeces. In small animals, there is vomiting.
Treatment: Ideal antidote is the specific antiserum but this is not
always available. Sedative along with glucose-saline IV drip is useful.
Injection of arecoline hydrobromide followed by saline purgatives may
also prove successful.

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 Sweet Clovers
 Melioltus officinalis (ASPURK, IKLEL-UL-MALIK)
 M. indicus (SENI ZARD)
 M. alba (SENII SAFED):
Poison: They contain the harmless substance coumarin. Sweet clover when damaged
by weather or when becomes mouldy, coumarin is broken down to dicoumarol which
acts as an anticoagulant by interfering with prothrombin production in liver.
Symptoms: Haemorrhages occur all over the body in cattle. sheep, and horses. There
is lameness, bloody diarrhoea, and some animals die suddenly. Warfarin and other
rodenticides also produce similar symptoms.
Treatment: Treatment is vitamin K injection or menaphthone (an analogue). Blood
transfusion is also useful.

14. Animal Poisons
 • Insects:
 1.Blister beetles:It causes cantharidin toxicosis. Cantharidin is used to treat
variety of illness. It is taken from hemolymph and genitalia of blister beetle.
 Mechanism of action: Cantharidin absorbed in GIT and excreted in urine.
Disruption of the membrane results in acantholysis(loss of coherence between
epidermal cells due to the breakdown of intercellular bridges) and vesicle
formation.
 Treatment: Activated charcoal may also bind cantharidin. Have supportive
treatment
 Clinical Sign: restlessness, depression, sweating, congested mucous
membranes. Common signs include fever, pollakiuria, and diarrhea.

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2.Fireflies:
 Fireflies of the genus Photinus contain steroidal pyrones called lucibufagins,
which are structurally related to the cardiotoxic bufodienolides (a type of
cardiac glycosides) and cardenolides of plants.
Mechanism of action:
They inhibit sodium–potassium ATPase activity in the myocardial cell
membrane in a mechanism similar to digitalis. However, because of their
structural similarity to bufodienolides and cardenolides.
Clinical sign:
Oral gaping, dyspnea, neck colour changes to black
Treatment: Because of the acute onset of signs, veterinary care could not be
instituted before death in any animals so far.

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 • Reptiles:
 1.Coral snakes Coral snakes are small, vibrantly colored, highly venomous snakes.
They have the second-strongest venom of any snake (the black mamba has the most
deadly venom)
 The snake’s neurotoxic venom causes rapid paralysis and respiratory failure in its
prey; however, according to the National Institutes of Health, it can take many hours
for symptoms to appear in humans. Additionally, there is often little or no pain or
swelling in humans from a coral snake bite
 Mechanism of action: Coral snake venom acts by inhibiting acetylcholine
receptors at the neuromuscular junction to cause neurotoxic motor weakness. Life-
threatening complications of coral snake bites are related to respiratory muscle
weakness and the need for ventilatory support.
 Treatment: Administration of antivenin (M.fulvius)
 Clinical sign: Decreased blood pressure, respiratory depression, loss of spinal
reflexes in all limbs, anisocoria, and hypothermia can also manifest

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 • Lizards:
 The venom is released from two venom glands on the lower jaw.
 Mechanism of action: The venom is a mixture of biologically active proteins. Venom
stimulates insulin secretion in response to increase in glycemia and modulate gastric
emptying to slow the entry of ingested sugar in the blood
 Clinical signs :Common symptoms include pain, swelling, and discoloration in the
area around the bite as well as swollen lymph nodes. Weakness, sweating, thirst,
headache, and ringing in the ears (tinnitus) may develop. In severe cases, blood
pressure may fall.
 Treatment:
 Wash the wound for 5 minutes with large amounts of clean warm water. Do not use
rubbing alcohol, hydrogen peroxide, iodine, or Mercurochrome, which can harm the
tissue and slow wound healing. Drench the wound in warm water for 20 minutes, 2 to
4 times a day, for the next 4 to 5 days.

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 • Pits Vipers:They are distinguished by the presence of a heat-sensing pit organ located
between the eye and the nostril on both sides of the head.
 This organ has the amazing ability to sense infrared heat to track prey.
 Pits viper have hemotoxic venom.
 Mechanism of action: The primary purpose of pit viper venom is to immobilize prey and
predigest victim’s tissues. The enzymatic fraction of the venom breaks down connective
tissue. Toxin cause bleeding or interfere with the blood or bloods ability to clot.
 Clinical sign: Swelling, hemorrhages, The venom of rattlesnakes and other pit vipers
damages tissue around the bite. Venom may cause changes in blood cells, prevent blood
from clotting, and damage blood vessels, causing them to leak. These changes can lead to
internal bleeding and to heart, respiratory, and kidney failure.
 Treatment: CroFab [Crotalidae polyvalent immune Fab (ovine)] (FabAV) is currently the
only FDA approved anti-venom for the treatment of pit viper bites. The recommended
dose for symptomatic pit viper bites range from 4-12 vials initially in both children and
adults depending on the presenting signs and symptoms.

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 • Spiders:
 1.Black widow: Toxin is α-latrotoxin. The venom of the black widow is potent, much
more so than the venomous snakes. It is thought that picomolar concentrations of the
venom can result in clinical intoxication.
 Mechanism of action: Black widow spider venom is an agonist (a chemical
substance that mimics or enhances the effects of a neurotransmitter) for ACh. The
venom of the black widow spider causes a flood of acetylcholine to be released into
the body's muscle system, causing convulsions.
 Clinical sign: The signs include muscle fasciculation and rigidity, abdominal pain,
ataxia, and flaccid paralysis.
 Treatment:
 Latrodectus mactans envenomation, Opioids (fentanyl) or benzodiazepines
(diazepam) have been recommended for the control of pain.

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 2.Brown Recluse:
 The venom has component 32-kD protein, sphingomyelinase.
 Mechanism of Action: The venom of the brown recluse spider is a complex
mixture of enzymes. The protein causes a disruption of cell membranes with
resulting microvascular damage and platelet aggregation. Brown Recluse have
shown degradation of basement membrane components. This action of the venom
was noted in the absence of neutrophils.
 Clinical sign:Dermal necrosis, Hemolysis, nausea, vomiting, fever, and
generalized malaise.
 Treatment: No specific antidote for brown recluse envenomation exists.
Syptomatic treatment for human envenomation includes dapsone, wound excision,
and hyperbaric oxygen therapy.

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 Scorpion:
 Mechanism:
 The primary targets of scorpion venom are voltage-dependent ion channels,(sodium
channels). Venom toxins alter these channels, leading to prolonged neuronal activity.
Many end-organ effects are secondary to this excessive excitation.
 Clinical sign at the site of the sting can include: intense pain, tingling and numbness
around the sting, swelling around the sting
 Symptoms related to widespread effects of venom can include: breathing difficulties,
muscle thrashing or twitching unusual movements of the neck, head, and eyes dribbling or
drooling sweating, nausea, vomiting, high blood pressure, accelerated heart rate or
irregular heartbeat, restlessness, excitability, or inconsolable crying
 Treatment: Anascorp (the first-ever FDA-approved scorpion anti venom)